AB1503 THE IMPACT OF OBESITY ON CLINICAL COURSE AND BIOLOGIC DMARD FAILURE IN PATIENTS WITH ADULT ONSET STILL’S DISEASE
Authors: I. DI Cola, F. Ursini, R. Giacomelli, P. Cipriani, P. Ruscitti
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Adult onset Still's disease (AOSD) is a rare inflammatory disease characterised by fever, arthritis, evanescent cutaneous rash and a typical hyperferritinemia [1]. Three clinical disease courses are usually identified: i. monocyclic, characterised by a single episode; ii. polycyclic, characterised by multiple flares, alternating with remission; iii. chronic, related to a persistent active disease [1]. AOSD may be also burdened by the occurrence of life-threatening complications. The prognosis of AOSD may be affected by the presence of comorbidities; however, the impact of obesity on these patients has not fully elucidated yet. The obesity may be considered as a negative prognostic factor in patients with rheumatic diseases. In fact, it is associated with a higher disease activity, an enhanced disability, and a less probability to achieve the clinical remission [2,3]. <h3>Objectives</h3> We assessed the impact of obesity on clinical disease course and biologic DMARD failure in patients with AOSD. We also evaluated the influence of obesity on life-threatening complication occurrence. <h3>Methods</h3> An assessment of obese patients with AOSD characterised by a BMI≥30 was provided among those evaluated in Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale (GIRRCS) cohort [4]. The presence of obesity was evaluated at the time of diagnosis and defined as BMI≥30. Cox regression analyses were performed to evaluate the predictive role of obesity on predicting different disease courses and bDMARD failure in our cohort. Multivariate analyses were adjusted for age, gender, and systemic score, which was used as marker of disease severity. <h3>Results</h3> In this study, 139 patients were evaluated; 26 (18.7%) had a BMI≥30 and were defined as having obesity at the time of disease diagnosis (mean age of 39.3±13.6 years, 12 male gender). Obese patients did not differ in the main clinical characteristics than non-obese [fever BMI≥30: 96.2% vs BMI&lt;30: 99.1%, p=0.340; skin rash BMI ≥ 30: 84.6% vs BMI&lt;30: 69.0%, p=0.147; arthritis BMI≥30: 61.5% vs BMI&lt;30: 56.6%, p=0.826]. Furthermore, obese patients showed a higher rate of bDMARD failure in the subsequent follow-up (p=0.037). In addition, obese patients with AOSD were characterized by higher values of C-reactive protein (CRP) [BMI≥30: 109.2 mg/L (IQR 117.0) vs BMI&lt;30: 52.0 mg/L (IQR 84.3), p=0.046] than others. Obese patients with AOSD had also higher values of CRP than 2:1 age-, gender-, and BMI-matched obese patients without immune mediated inflammatory disease (IMID) (Age: 39.8 ± 13.2 years, 24 male gender out 52 patients, BMI: 32.4 ± 3.1, CRP 33.8 mg/L [IQR 34.4], p&lt;0.001). These obese patients without IMID were recruited to fully evaluate the impact of obesity on CRP in patients with AOSD. Additionally, obesity predicted the development of a chronic disease course in patients with AOSD in both univariate (HR: 1.72, 95%CI: 1.03-2.51, p=0.038) and multivariate analyses (HR: 1.85, 95%CI: 1.45-2.89, p=0.041). Non-significant results were obtained assessing the predictive role of obesity on monocyclic and polycyclic disease courses. Furthermore, obesity resulted to be a significant predictor of failure of at least one of biologic DMARD in patients with AOSD in both univariate (HR: 3.03, 95%CI: 1.42-6.45, p=0.004) and multivariate analyses (HR: 3.59, 95%CI: 1.55-8.27, p=0.003). Conversely, obesity did not influence the development of life-threatening complications in our cohort. <h3>Conclusion</h3> The presence of obesity resulted to be a predictive factor for the development of a chronic disease course and biologic DMARD failure in patients with AOSD. In addition to increase the inflammatory burden, a high BMI may be indeed associated with a more rapid clearance, a higher volume of distribution, and a consequent low concentration of biologic DMARDs and their possible clinical failure. <h3>References</h3> [1]Giacomelli R, et al. J Autoimmun. 2018; 93:24-36 [2]Shan J, et al. Joint Bone Spine. 2019;86:173-83 [3]de Resende Guimarães MFB, et al. Adv Rheumatol. 2019;59:44 [4]Ruscitti P, et al. Rheumatology (Oxford). 2022; 61:4124-9 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.